**1. Introduction**

The discovery of the gu<sup>t</sup> microbiota universe and the growing understanding of its role in health and disease have radically changed the current point of view on the pathogenesis of noncommunicable diseases [1]. Among these, celiac disease (CD) represents a privileged situation since both the external (gluten) and internal (tissue transglutaminase) antigens as well as the predisposing human leukocyte antigen haplotypes have been identified [2]. However, although gluten is widely ingested, tissue transglutaminase is a ubiquitous enzyme, and the frequency of at-risk alleles in the general population approaches 40%, only a small proportion of subjects eventually develop enteropathy [3]. Additional factors have therefore been invoked to explain the onset and maintenance of loss of gluten tolerance and mucosal damage. Recently, evidence has been accumulated on the presence of perturbations of the microbiota composition [4] not only in active CD (ACD) [5] but also in a consistent proportion of treated patients (TCD) [6]. Whether dysbiosis represents an epiphenomenon of the enteropathy or, conversely, it contributes to the development of mucosal damage still remains unknown.

On this basis, we firstly aimed to characterize the mucosal microbiota of an adult CD population, including ACD, TCD, refractory CD (RCD), and potential CD (PCD), and compare it to non-CD controls by using the amplicon metagenomics approach. Secondly, since it is unlikely that the most studied bacterial consortium, i.e., fecal microbiota, represents the composition at the level of duodenal mucosa, we also collected and analysed salivary samples to assess whether they mirror the profile at mucosal level better than feces.

#### **2. Patients and Methods**
